Alzheimer's disease is characterized by the accumulation of a 39-43 amino acid peptide termed the beta-amyloid protein or Aβ, in a fibrillar form, existing as extracellular amyloid plaques and as amyloid within the walls of cerebral blood vessels. Fibrillar Aβ amyloid deposition in Alzheimer's disease is believed to be detrimental to the patient and eventually leads to toxicity and neuronal cell death, characteristic hallmarks of Alzheimer's disease. Accumulating evidence now implicates amyloid as a major causative factor of Alzheimer's disease pathogenesis. Discovery and identification of new compounds, agents, proteins, polypeptides or protein-derivatives as potential therapeutic agents to arrest Alzheimer's disease Aβ amyloid formation, deposition, accumulation and/or persistence is desperately sought.
It is known that Aβ is normally present in human blood and cerebrospinal fluid. However, it is not known why this potential fibrillar protein remains soluble in circulating biological fluids. Can the agent(s) responsible for this extraordinary solubility of fibrillar Aβ be applied to diagnostic and therapeutic regimens against the fibrillar Aβ amyloid present in Alzheimer's brain?